This document discusses trauma from occlusion (TFO), which refers to pathologic alterations or adaptive changes in the periodontium resulting from excessive occlusal forces. It covers the historical understanding of TFO, definitions, classifications, clinical features, and the periodontal response and adaptation to excessive forces. It also examines Glickman's concept of co-destruction between TFO and plaque-associated periodontal disease. The document provides details on injury, repair, remodeling processes in the periodontium in response to TFO.

1. TRAUMA FROM OCCLUSION

2. CONTENTS
 INTRODUCTION
 HISTORICAL ASPECTS
 DEFINITIONS
 CLASSIFICATION
 CLINICAL FEATURES
 PERIODONTAL RESPONSE TO EXCESSIVE OCCLUSAL FORCES

 INJURY
 REPAIR
 ADAPTIVE REMODELLING OF THE PERIODONTIUM
 TRAUMA FROM OCCLUSION AND PLAQUE-ASSOCIATED PERIODONTAL DISEASE
 GLICKMANS’ CONCEPT (THEORY OF CO-DESTRUCTION)
WAERHAUG CONCEPT
 CLINICAL TRIALS
 HUMAN TRIALS
 ANIMAL TRIALS
 TFO AROUND IMPLANTS
 PATHOLOGICAL TOOTH MIGRATION
 EFFECT OF TFO ON DENTAL PULP
 EFFECETS OF INSUFFICIENT OCCLUSAL FORCES
 REVERSIBILITY OF TRAUMATIC LESIONS
 LITERATURE REVIEWS
 DIAGNOSIS
 TREATMENT ASPECTS
 CONCLUSION
 REFERENCES

3. INTRODUCTION
 For many years, the role of occlusion and its dynamic interactive impact on the periodontium has been an
issue of controversy and extensive debate. Although a variety of occlusal conditions have purportedly
been related to this interaction, the central focus has been on occlusal trauma resulting from excessive
forces applied to the periodontium
 Trauma from occlusion is a term used to describe pathologic alterations or adaptive changes which develop
in the periodontium as a result of undue force produced by the masticatory muscles.
 Trauma from occlusion is only one of many terms that have been used to describe such alterations in the
periodontium.
 In addition to producing damage in the periodontal tissues, excessive occlusal force may also cause injury
in, for example, the temporomandibular joint, the masticatory muscles, and the pulp tissue.

4. HISTORICAL ASPECT
4
Karolyi (1901) –
Postulated interaction
between TFO &
“alveolar pyrrohea”
Stillman (1917 &
1926) – Advocated
use of occlusal
adjustment for
treatment of TFO
Box & Stones
(1930’s ) - Animal
experiments TFO
etiologic factor in
periodontal disease
Orban & Weinman
(1933) - Occlusal
forces did not have a
major effect on
periodontal
destruction.
Glickman and co-
workers (1960s ) -
Performed a series
of animal model and
human autopsy
studies
Goldman et al in an
experimental animal
study, evaluated the
effects of occlusal
trauma on gingival
blood flow.
Stahl (1968) –
Evaluated the
interaction between
occlusal trauma and
plaque-induced
periodontal
inflammation.
Waerhaug (1979)-
Evaluated the
relationship of the
morphology of the
bone & pocket with
the plaque level and
presence or absence
of excessive occlusal
forces.

5. DEFINITIONS
5
Other terms often used are: traumatizing occlusion, occlusal trauma, traumatogenic occlusion, periodontal
traumatism, overload, etc.
 STILLMANN “a condition where injury results to the supporting structures of the teeth by the act of
bringing the jaws into a closed position
When occlusal forces exceed the adaptive
capacity of the tissues, tissue injury results.this
resultant injury is termed TFO. (Glickman)
STILLMANN “a condition where injury results to
the supporting structures of the teeth by the act
of bringing the jaws into a closed position
Damage in the periodontium caused by stress
on the teeth produced directly or indirectly by
teeth of the opposing jaw. (WHO,1978)
An injury to the attachment apparatus as a
result of excessive occlusal force.
(Glossary of periodontic terms AAP,1992)

6. CLASSIFICATION
6
 Glickman’s classification (1953)
 According to duration of cause:
 i. Acute TFO
 ii. Chronic TFO.
 According to nature of cause:
 i. Primary TFO
 ii. Secondary TFO.
 Box’s classification
 Physiologic occlusion
Box defined it as a condition, in which the systems of forces acting upon the tooth during the occlusion are in a state of equilibrium, and they do not and cannot
change the normal relationship existing between the tooth and its supporting structures.
 Traumatic occlusion
The damage produced in the periodontium is due to the overstress produced by the occlusion

7. 7
•Acute Trauma
•Occurs on abrupt occlusal impact.
•Caused by restorations or prosthetic appliances that interfere with
or alter the direction of occlusal forces on the teeth.
•Results in tooth pain, sensitivity to percussion and increased tooth
mobility
ACUTE
TRAUMA
•Chronic Trauma
•It is more common than acute and is of greater clinical significance.
•Caused by gradual changes in the occlusion produced by tooth wear,
drifting movement and extrusion of teeth combined with para-
functional habits such as bruxism and clenching.
CHRONIC
TRAUMA

8. 8
When trauma to the supporting tissues occurs as a result of alterations in occlusal forces, it is called primary TFO.
•High filling
•Prosthetic replacement creating excessive forces
•Drifting or extrusion of teeth
•Orthodontic movement into functionally unacceptable oppositions
In primary TFO there are no changes in the level of connective tissue attachment and no pocket formation
Secondary TFO Occurs when, the adaptive capacity of the tissues to withstand occlusal
forces is impaired by bone loss resulting from marginal inflammation.
 This reduces the periodontal attachment area and alters the leverage on the remaining
tissues.
 The periodontium becomes vulnerable to injury, and previously well tolerated forces
become traumatic.
 Combined occlusal trauma refers to injury resulting from abnormal occlusal forces applied
to a tooth or teeth with inadequate (abnormal) periodontal support

9. 9
 1. Normal periodontium with normal height of bone
 2. Normal periodontium with reduced height of bone
 3. Marginal periodontitis with reduced height of bone
 It has been found in experimental animals that systemic disorders can reduce tissue resistance and that previously
tolerable forces may become excessive. This could theoretically represent
another mechanism by which tissue resistance to increased forces is lowered, thereby resulting in secondary
trauma from occlusion

10. The signs and symptoms of chronic trauma from
occlusion include (AAP, 2000).10
 Tooth mobility
 Tooth migration
 Tooth pain or discomfort on chewing or percussion
 Widening of the PDL, disruption of the lamina dura, radiolucency in the furcation or at the apex of
vital teeth, root resorption as observed in intra-oral X-rays images
 Tenderness of mastication muscles and/or TMJ dysfunction
 Presence of wear facets beyond levels expected for patient’s age or diet
 Chipped enamel or crown/root factures
 Increased width of periodontal ligament space, often with thickening of the lamina dura along the
lateral aspect of the root, in the apical and furcation areas,
 Angular bone loss, mainly at the coronal level of interdental septum, with a funnel-shaped
morphology
 Radiolucency lamina dura surrounding the angular bone loss, resembling an infrabony defect
 Condensation of the alveolar bone can be produced after widening of the periodontal ligament
 Root resorption

11. INFLUENCE OF OCCLUSION ON THE
PERIODONTIUM11
 CLINICAL FEATURES
 Progressive mobility
 Fremitus
 Wear facets
 Occlusal discrepencies
 Fractured tooth
 Thermal sensivity

12. 12
 Fremitus is a measurement of the vibratory patterns of the teeth when
the teeth are placed in contacting positions and movements.
 A dampened index finger is placed along the buccal and labial surfaces
of the maxillary teeth, and patient is asked to tap the teeth together in
the maximum ICP and grind systemically in the lateral, protrusive, and
lateral protrusive contacting movements and positions
 • Class 1: Mild vibration or movement detected
 • Class II: Easily palpable vibration but no visible movement
 • Class III: Movement visible with the naked eye.

13. Radiographic features
13
 Increased width of the periodontal space, often
with thickening of the lamina dura along the
lateral aspect of the root, in the apical region, and
in the bifurcation areas.
 A vertical destruction of the interdental septum
 Root resorption.
 Lipping

14. Gingival recession??
14
 Although it has been speculated that the elimination of trauma by occlusal adjustment, relieving
the incidence of excessive occlusal force on teeth showing gingival cleft formation, resulted in
spontaneous remission of gingival recession, with no additional treatment performed
 Furthermore, no relationship was found between the existence of occlusal discrepancies, whether
treated or not, and changes in keratinized gingiva width, as described by Harrel and Nunn
 A recent systematic review to investigate the role of traumatic occlusion in the initiation and
progression of gingival recessions was performed, in an attempt to gain a clearer understanding of
the role of occlusion in these lesions
 It could be concluded that the relationship between the conditions remains as “a clinical opinion”
and that it seemed convenient to control occlusal factor in clinical practice because it can be
considered as an independent risk factor for periodontal disease

15. ADAPTIVE CAPACITY OF THE PERIODONTIUM TO OCCLUSAL
FORCES
15
Magnitude :
When occlusal force is increased, the periodontium
a thickening of the periodontal ligament,
an increase in the number and width of the PDL fibers
an increase in the density of alveolar bone.
2. Direction : reorientation of the stresses and strains
The principal fibers of the PDL are arranged so that they best
accommodate occlusal forces along the axis of the tooth .
Lateral (horizontal) & torque (rotational) forces more injurious
3. Duration :
Constant pressure Intermittent force
4 . Frequency
more frequent

16. PERIODONTAL RESPONSE TO EXCESSIVE OCCLUSAL FORCES
16
 Tissue response occurs in three stages:
 Injury
 Repair and
 Adaptive remodeling of the periodontium

17. Tissue injury
17
 Tissue injury is produced by excessive occlusal forces. The body then
attempts to repair the injury and restore the periodontium.
 This can occur if the forces are diminished or if the tooth drifts away from
them. If the offending force is chronic, however, the periodontium is
remodeled to cushion its impact.
 The ligament is widened at the expense of the bone, which results in
angular bone defects without periodontal pockets, and the tooth becomes
loose.

18. 18
 Under the forces of occlusion, a tooth rotates around a fulcrum or axis of
rotation, which in single-rooted teeth is located in the junction between the
middle third and the apical third of the clinical root and in multirooted teeth in
the middle of the interradicular bone .
 This creates areas of pressure and tension on opposite sides of the fulcrum.
 Different lesions are produced by different degrees of pressure and tension. If
jiggling forces are exerted, these different lesions may coexist in the same area.

19. 19
 Slightly excessive pressure stimulates resorption of the alveolar bone, with a
resultant widening of the periodontal ligament space.
 Slightly excessive tension causes elongation of the periodontal ligament fibers and
the apposition of alveolar bone.
 In areas of increased pressure, the blood vessels are numerous and reduced in
size; in areas of increased tension, they are enlarged.

20. 20

21. 21

22. 22

23. 23
 The areas of the periodontium that are most susceptible to injury from
excessive occlusal forces are the furcations.
 Injury to the periodontium produces a temporary depression in mitotic
activity, in the rate of proliferation and differentiation of fibroblasts,in
collagen formation, and in bone formation
 These return to normal levels after the dissipation of the forces.

24. ORTHODONTIC TYPE TRAUMA
24
 When a tooth is exposed to unilateral forces of a magnitude, frequency or duration that its
periodontal tissues are unable to withstand and distribute while maintaining stability of the tooth,
certain well-defined reactions develop in the periodontal structures to the altered functional
demand
 When horizontally directed forces are applied, the tooth tilts in direction of the force resulting in
the development of pressure and tension zones within the marginal and apical parts the tooth
becomes hypermobile temporarily, moves to a new position and healing takes place.
 If the crown of the tooth is effected by such horizontally directed forces, eventually results in
adaptation of periodontal structures to functional demand.
 In this tissue reaction, bone resorbing osteoclasts soon appear on the bone surface of the alveolus
in the pressure zone. A process of bone resorption is initiated. This phenomenon is called direct
bone resorption.

25. 25
 Forces in one direction: orthodontic forces
 In the periodontal ligament, zone of compression
 zone of tension
 temporary increased mobility (functional adaptation
).
 no changes in the supracrestal fibres,
 no loss of periodontal attachment,
 no increased probing pocket depth.
 Forces too high (above the adaptation level),
 aseptic necrosis of the PDL.
 root resorption occurs
 resulting in shorter roots.

26. Tipping movement
26

27. Bodily movement
27

28. INDIRECT BONE RESRPTION
28
 If the force applied is of higher magnitude, the result may be necrosis of the
periodontal ligament tissue in the pressure zone, i.e. decomposition of cells, vessels,
matrix, and fi bers (hyalinization). “
 Direct bone resorption” therefore cannot occur. Instead, osteoclasts appear in marrow
spaces within the adjacent bone tissue where the stress concentration is lower than in
the periodontal ligament and a process of undermining or “indirect bone resorption” is
initiated.
 Through this reaction the surrounding bone is resorbed until there is a breakthrough to
the hyalinized tissue within the pressure zone.

 Irrespective of whether the bone resorption is of a direct or an indirect nature the
tooth moves (tilts) further in the direction of the force.

29. TRAUMA JIGGLING TYPE
29
 Alternate traumatic forces are applied in buccal and lingual directions or
mesial and distal directions so that the teeth are not allowed to move away
from the force.
 There is a combination of pressure and tension zones associated with
increased width of the PDL space on both sides, leading to inflammatory
changes, active bone resorption and progressive mobility.
 (Wentz et al. 1958;Glickman & Smulow 1968; Svanberg & Lindhe 1973; Meitner 1975; Ericsson &
Lindhe 1982).
 At one stage, when the increasing width reaches a level where it compensates for
the forces, the teeth are hypermobile but mobility is no longer progressive

30. Jiggling type of trauma
30

31. Healthy periodontium with reduced bone height
31

32. Periodontitis with reduced bone height
32

33. 33 In presence of plaque-associated periodontal disease, the tissues in
the pressure/tension zones could not become adapted and the
injury in the zones of co-destruction had a more permanent
character.
 Continuous alveolar bone destruction
 Mobility of the teeth remained progressive
 Merging of the zone of irritation and the zone of co-destruction
 Dentogingival epithelium proliferated apically and periodontal
disease was aggravated.
 In conjunction with “jiggling type of trauma” no clear cut pressure
and tension sites can be identified but rather there a combination of
pressure and tension on both sides of the jiggled tooth

34. STAGE 11 REPAIR
34
 Repair occurs constantly in the normal periodontium, and trauma from
occlusion stimulates increased reparative activity.
 The damaged tissues are removed, and new connective tissue cells and
fibers, bone, and cementum are formed in an attempt to restore the
injured periodontium .
 Forces remain traumatic only as long as the damage produced exceeds the
reparative capacity of the tissues.

35. Buttressing bone formation
35 Excessive occlusal forces…. resorption of bone…. Body reinforces the thinned bony trabeculae with new
bone…Buttressing bone formation
CENTRAL
Endosteal cells
deposit
new bone
Restores bony
trabeculae &
reduces the size of
marrow spaces
PERIPHERAL
Shelf like
thickening of the
alveolar margin
LIPPING
Bulge in the
contour of the
facial & lingual
bone

36. Stage III: Adaptive Remodeling of the
Periodontium36
 If the repair process cannot keep pace with the destruction caused by the
occlusion, the periodontium is remodeled in an effort to create a structural
relationship in which the forces are no longer injurious to the tissues.
 This results in a widened periodontal ligament, which is funnel shaped at
the crest, and angular defects in the bone, with no pocket formation. The
involved teeth become loose.
 Increased vascularization has also been reported

37. HISTOMETRIC ANALYSIS
37
 The three stages in the evolution of
traumatic lesions have been
differentiated histometrically by the
relative amounts of periodontal bone
surface undergoing resorption or
formation
 The injury phase shows an increase in
areas of resorption and a decrease in
bone formation, whereas the repair
phase demonstrates decreased
resorption and increased bone
formation.
 After adaptive remodeling of the
periodontium, resorption and formation
return to normal.

38. Relationship Between Plaque-InducedPeriodontal Diseases and Trauma
From Occlusion
38
 The clinical impressions of early investigators and clinicians
assigned an important role to TFO in the etiology of periodontal
lesions. Numerous studies have since been performed to determine
the mechanisms by which TFO may affect periodontal disease.
 These studies can be classified broadly into three categories: -
 Human autopsy material
 Clinical trials
 Animal experiments

39. HUMAN AUTOPSY MATERIAL
39
 Certain criteria were evaluated using human autopsy material.
They were
 Histopathology of the lesions
 Presence of apical extension of microbial deposits
 Mobility
 Occlusion
 Based on these findings, two concepts were proposed: -
 Glickmans concept- Theory of Co-destruction.
 Waerhaug concept

40. Glickman’s concept
40
 Glickman (1965, 1967) claimed
that the pathway of the spread of a
plaque-associated gingival lesion
can be changed if forces of an
abnormal magnitude are acting on
teeth harboring subgingival plaque.
 Based on this concept, the
periodontal structures can be
divided into two zones: -
 Zone of irritation
 Zone of co-destruction
Zone of irritation and co-destruction

41. 41
 The zone of irritation includes the marginal and
interdental gingiva. The soft tissue of this zone is
bordered by hard tissue (the tooth) only on one side
and is not affected by forces of occlusion.
 This means that gingival infl ammation cannot be
induced by trauma from occlusion but is the result of
irritation from microbial plaque.
 The zone of co-destruction includes the periodontal
ligament, the root cementum, and the alveolar bone,
and is coronally demarcated by the trans-septal
(interdental) and the dento-alveolar collagen fi ber
bundles . The tissue in this zone may become the seat
of a lesion caused by trauma from occlusion.

42. 42
 Through this exposure from two different directions the fiber bundles may
become dissolved and/or orientated in a direction parallel to the root
surface.
 The spread of an infl ammatory lesion from the zone of irritation directly
down into the periodontal ligament (i.e. not via the interdental bone) may
hereby be facilitated
 This alteration of the “normal” pathway of spread of the plaque-associated
infl ammatory lesion results in the development of angular bony defects.

43. Waerhaugs concept
43
 Waerhaug (1979) examined autopsy specimens similar to Glickman’s, but in addition
measured
 the distance between the subgingival plaque and
 (1) the periphery of the associated infl ammatory cell infi ltrate in the gingiva, and
 (2) the surface of the adjacent alveolar bone.
 He concluded from his analysis that angular bony defects and infrabony pockets occur
equally often at periodontal sites of teeth which are not affected by trauma from
occlusion as in traumatized teeth.
 In other words, he refuted the hypothesis that trauma from occlusion played a role in
the spread of a gingival lesion into the “zone of codestruction”.

44. 44
 Loss of connective tissue attachment and the resorption of bone
around teeth are exclusively the result of inflammatory lesions
associated with subgingival plaque.
 Angular bony defects and infrabony pockets occur when the
subgingival plaque of tooth has reached a more apical level than the
microbiota of the neighboring tooth and the volume of the alveolar
bone surrounding the roots is comparatively large.

45. HUMAN TRIALS
45Rosling et al, 1976: The infrabony pocket located at hypermobile teeth exhibited the same degree healing as
those adjacent to firm teeth.
Fleszar et al, 1980: Pockets of clinically mobile teeth do not respond as well to periodontal treatment as those of
firm teeth exhibiting the same disease activity
Richard A. Reinhardt et.al, 1984, used a mathematical system (finite element anaiysis) to calculate principal
periodontal ligament stresses in primary and secondary occlusal trauma. The periodontal ligament appears to
play a significant role in modulating the stresses transmitted from the root to the bone.
Philstrom et al, 1986: teeth with increased mobility and widened PDL space had, in fact, deeper pockets, more
attachment loss and less bone support than teeth without these symptoms.
Burgett et al: Probing attachment gain was on the average about 0.5mm larger in patients who received scaling
and occlusal adjustment than in patients in whom the occlusal adjustment was not included.
Neiderud et al, 1992: Tissue alterations which occur at mobile teeth with clinically healthy gingival may reduce
the resistance offered by the periodontal tissues to probing.
A recent retrospective study (Harrel et al. 2001) showed that: teeth with occlusal discrepancies had deeper PDs
and worse prognosis occlusal adjustment improved the prognosis

46. ANIMAL TRIALS
46
 Rochester Group (Polson and co workers)
 Used squirrel monkeys
 Used mesial-distal compression forces (orthodontic type)
 Experimental times up to 10 weeks
 Occlusal trauma does not influence periodontal disease
progression (No evidence of attachment loss in the presence of
plaque and occlusal forces)

47. 47
 Gothenburg Group (Lindhe and co workers)
 Used beagle dogs
 Applied buccal-lingual forces using a cap splint (jiggling type)
 Experimental times up to one year
 Occlusal trauma could accelerate the progression of periodontal disease (Evidence
of attachment loss when plaque and occlusal forces were both present)
 This group found that occlusal stresses increase the periodontal destruction
induced by periodontitis.

48. Other theories
48 Trauma from occlusion may alter the pathway of the extension of gingival inflammation to
the underlying tissues. This may be favored by the reduced collagen density and the
increased number of leukocytes, osteoclasts, and blood vessels in the coronal portion of
increasingly mobile teeth. inflammation may then proceed to the periodontal ligament rather
than to the bone. Resulting bone loss would be angular, and pockets could become intrabony.
 • Trauma-induced areas of root resorption uncovered by apical migration of the inflamed
gingival attachment may offer a favorable environment for the formation and attachment of
plaque and calculus and therefore may be responsible for the development of deeper lesions.
• Supragingival plaque can become subgingival if the tooth is tilted orthodontically or if it
migrates into an edentulous area, which results in the transformation of a suprabony pocket
into an intrabony pocket.
 • Increased mobility of traumatically loosened teeth may have a pumping effect on plaque
metabolites, thereby increasing their diffusion.

49. 49

50. 50

51. 51

52. 52
There is no scientific
evidence to show that
trauma from occlusion
causes gingivitis or
periodontitis or
accelerates the
progression of gingivitis
to periodontitis.
• The periodontal
ligament physiologically
adapts to increased
occlusal loading by
resorption of the alveolar
crestal bone, resulting in
increased tooth mobility.
This is occlusal trauma
and is reversible if the
occlusal force is reduced.
• Occlusal trauma may be
a cofactor which can
increase the rate of
progression of an existing
periodontal disease
There is a place for
occlusal therapy in the
management of
periodontitis, especially
when related to the
patient's comfort and
function.
• Occlusal therapy is not
a substitute for
conventional methods of
resolving plaque-induced
inflammation.

53. MALOCCLUSION ARE TRAUMATIC???
53
The criterion that determines whether an occlusion is traumatic is whether it produces periodontal injury, not
how the teeth occlude.
Malocclusion is not necessary to produce trauma; periodontal injury may occur when the occlusion
appears normal.
Because trauma from occlusion refers to the tissue injury rather than to the occlusion, an increased
occlusal force is not traumatic if the periodontium can accommodate it.

54. EFFECTS OF EXCESSIVE OCCLUSAL FORCESON DENTAL PULP
54
 The effects of excessive occlusal forces on the dental pulp have not been
established. Some clinicians report the disappearance of pulpal symptoms after
the correction of excessive occlusal forces.
 Pulpal reactions have been noted in animals subjected to increased occlusal forces,
but these did not occur when the forces were minimal and occurred over short
periods

55. PATHOLOGICAL TOOTH MIGRATION
55
Refers to tooth displacement that results when the balance among the factors
that maintain physiologic tooth position is disturbed by periodontal disease.
may occur in association with gingival inflammation and pocket formation
as the disease progresses.
most frequently in the anterior region…
usually accompanied by mobility and rotation.
migration in the occlusal or incisal direction is termed extrusion.

56. 56
Pathogenesis
Two major factors play a role in maintaining the normal position of the teeth:
1. Health and normal height of the periodontium and
2. Forces exerted on the teeth.
latter includes the forces of occlusion and pressure from the lips, cheeks, and
tongue

57. 57
FAILURE TO REPLACE FIRST MOLARS.
1. Second and third molars tilt, resulting in a decrease in vertical dimension
2. PM move distally, and the mandibular incisors tilt or drift lingually. While drifting distally, the
mandibular premolars lose their intercuspating relationship with the maxillary teeth and may
tilt distally.
3. Anterior overbite is increased. Mandibular incisors strike the maxillary incisors near the
gingiva or traumatize the gingiva.
4. The maxillary incisors are pushed labially and laterally
5. The anterior teeth extrude because the incisal apposition has largely disappeared.
6. Diastemata are created by the separation of the anterior teeth

58. TFO AROUND IMPLANTS
58
 An osseointegrated implant is direct contact with the sarrounding bone
 It has been suggested that functional load on dental implant may enhance
osseointegration and not result in the marginal bone loss when the occlusal
load is adequately distributed
 But occlusal overload adversly effects the implant stability
 It has been suggested by human and animal studies that occlusal overload may
cause the loss of osseointegration and early implant failure

59. Effects of Insufficient Occlusal Force
59
 Insufficient occlusal force may also be injurious to the supporting
periodontal tissues.
 Insufficient stimulation causes thinning of the periodontal ligament,
atrophy of the fibers, osteoporosis of the alveolar bone, and a reduction in
bone height.
 Hypofunction can result from an open-bite relationship, an absence of
functional antagonists, or unilateral chewing habits that neglect one side
of the mouth

60. Reversibility of Traumatic Lesions
60
 Trauma from occlusion is reversible.
 When trauma is artificially induced in experimental animals, the teeth move away or intrude into
the jaw.
 When the impact of the artificially created force is relieved, the tissues undergo repair.
 Although trauma from occlusion is reversible under such conditions, it does not always correct
itself, and therefore it is not always temporary or of limited clinical significance.
 The injurious force must be relieved for repair to occur.
 If conditions in humans do not permit the teeth to escape from or adapt to excessive occlusal force,
periodontal damage persists and worsens.
 The presence of inflammation in the periodontium as a result of plaque accumulation may impair
the reversibility of traumatic lesions.

61. 61
 Trauma from occlusion also tends to change the shape of the alveolar crest. The change
in shape consists of a widening of the marginal periodontal ligament space, a narrowing
of the interproximal alveolar bone, and a shelflike thickening of the alveolar margin.
 Therefore although trauma from occlusion does not alter the inflammatory process, it
changes the architecture of the area around the inflamed site.
 Thus in the absence of inflammation, the response to trauma from occlusion is limited
to adaptation to the increased forces.

 In the presence of inflammation, however, the changes in the shape of the alveolar crest
may be conducive to angular bone loss, and existing pockets may become intrabony.

62. Diagnosis
62
 Cardinal manifestation of
 primary TFO is increased tooth mobility.
 2. Tilting and migration of individual teeth or of complete segments.
 Careful palpation of the muscles of mastication to ascertain whether there
is hypertrophy or sign of hypertonicity with possible spasm of one group
of muscle
 4. Palpation of TMJ and observation of any deviation of the mandible in
various paths of closure
 5. Fremitus test

63. MANAGEMENT OF TRAUMA FROM OCCLUSION63
 Occlusal Analysis: Occlusion analysis is the study of the
relationship of the occlusal surfaces of opposing teeth and
their associated functional harmonies
 Occlusal registration steps
 Occlusal indicator wax
 Articulating paper, blue.(40-80 microns)
 Occlusal Contact Detection Instruments
 Occlusal sonography

64. DIFFERENT TREATMENT MODALITIES64
 Occlusal Adjustment – Coronoplasty
 Orthodontic Treatment
 Splinting
 Temporary
 Provisional
 Biteplanes

65. SEQUENCE FOR CORONOPLASTY
65
Step 1: Remove
retrusive
prematurities
and eliminate
the deflective
shift from RCP
to ICP
Step 2: Adjust
ICP to achieve
stable,
simultaneous,
multipointed,
widely
distributed
contacts.
Step 3: Test for
excessive
contact
(fremitus) on
the incisor
teeth.
Step 4: Remove
posterior
protrusive
supracontacts
and establish
contacts that
are bilaterally
distributed on
the anterior
teeth.
Step 6: Reduce
excessive cusp
steepness on
the
laterotrusive
(worki
ng) contacts.
Step 7:
Eliminate gross
occlusal
disharmonies.
Step 8:
Recheck
tooth contact
relationships.
Step 9: Polish
all rough
tooth
surfaces

66. TREATMENT CONSIDERATIONS
66
 The goals of the treatment of occlusal traumatism may
be described as:
1. elimination or reduction of tooth mobility
2. establishment or maintenance of a stable and reproducible maximal
intercuspal habitual position;
3. provision of efficient masticatory function
4. a comfortable occlusion with acceptable phonation and esthetics
5. elimination or modification of parafunctional habits.

67. 67
 Treatment of occlusal trauma may be performed at any phase of
periodontal therapy.
 For chronic periodontitis, treatment efforts are directed toward
elimination or minimization of excessive forces, and occlusal
therapy may be accomplished through several differentapproaches
 occlusal adjustment;
 management of parafunctional habits;
 temporary, provisional, or long-term stabilization of mobile teeth;
orthodontic tooth movement; and occlusal reconstruction or
extraction of selected teeth, depending on the case.

68. 68
 Treatment of primary or secondary trauma from occlusion requires controlling marginal inflammation
and restoring normal occlusal function.
 Remission of primary trauma from occlusion proceeds uneventfully if periodontal pockets are
successfully treated.
 Considering that, treatment of primary trauma from occlusion should basically address the occlusal
adjustment to redirect occlusal forces, allowing reversibility of the lesion.
 In cases n which periodontitis and trauma from occlusion coexist without producing a combined lesion,
treatment should be directed to the independent treatment of both conditions as two distinct pathological
entities.
 Occlusal adjustment should be performed, when indicated, 45 days prior to periodontal surgery in order
to allow rebuilding of existent bone matrix and prevent its loss during surgical debridement of
periodontal defects

69. 69

70. 70

71. 71

72. CONCLUSION
72
 In the field of periodontics, it seems crucial to prevent, treat, and maintain the periodontal
supporting apparatus, which is responsible for the long-term stability of teeth.
 Accepting this concept, periodontal treatment should be directed at the preservation of
periodontal supporting tissues, the homeostatic behavior of which may be dependent on the
proper distribution and neutralization of applied mechanical forces.
 Most of the research to investigate the role of occlusion in periodontics has been performed
in animal models or cadavers and hence does not reflect the real influence of trauma from
occlusion in humans.
 As a consequence, aggravation of plaque-related inflammatory periodontal disease by
trauma from occlusion is still under question, and further investigations are necessaryto
elucidate such an association.

73. REFERENCES
73
 Carranza’s Clinical Periodontology; 8th editi; 10 and 13th edition
 Clinical Periodontology and Implantology;4th and fifth and 6 thedition; Jan Lindhe
 Trauma from Occlusion: The Overstrain of the Supporting Structures of the Teeth Dhirendra
Kumar Singh, Md. Jalaluddin, Rajeev Ranjan Indian Journal of Dental Sciences 2017
 Role of occlusion in periodontal disease Euloir Passanezi , Adriana Campos Passanezi
Sant'Ana Periodontology 2000. 2019;79:129–150.
 Trauma from occlusion — An orthodontist’s perspective R. Saravanan, Prajeeth J. Babu, P.
Rajakumar Journal of Indian Society of Periodontology - Vol 14, Issue 2, Apr-Jun 2010
 Occlusal considerations in periodontics S. J. Davies,1 R. J. M. Gray,2 G. J. Linden,3and J. A.
James, BRITISH DENTAL JOURNAL, VOLUME 191, NO. 11, DECEMBER 8 2001